Abstract

BACKGROUND:

Upon appropriate stimulation, plants increase their level of resistance against future pathogen attack. This phenomenon, known as induced resistance, presents an adaptive advantage due to its reduced fitness costs and its systemic and broad-spectrum nature. In Arabidopsis, different types of induced resistance have been defined based on the signaling pathways involved, particularly those dependent on salicylic acid (SA) and/or jasmonic acid (JA).

RESULTS:

Here, we have assessed the implication of the transcriptional regulator OCP3 in SA- and JA-dependent induced defenses. Through a series of double mutant analyses, we conclude that SA-dependent defense signaling does not require OCP3. However, we found that ocp3 plants are impaired in a Pseudomonas fluorescens WCS417r-triggered induced systemic resistance (ISR) against both Pseudomonas syrinagae DC3000 and Hyaloperonospora arabidopsidis, and we show that this impairment is not due to a defect in JA-perception. Likewise, exogenous application of JA failed to induce defenses in ocp3 plants. In addition, we provide evidence showing that the over-expression of an engineered cytosolic isoform of the disease resistance regulator NPR1 restores the impaired JA-induced disease resistance in ocp3 plants.

CONCLUSIONS:

Our findings point to a model in which OCP3 may modulate the nucleocytosolic function of NPR1 in the regulation of JA-dependent induced defense responses.

OCP3 is not implicated in the SA-dependent disease resistance signaling against P. syringae. Five-week-old plants were challenge inoculated with a bacterial suspension of virulent Pst DC3000 at the concentration of OD600 = 0.0004 (a) (Infiltration) or OD600 = 0.2 (b) (Spray). Three days after challenge inoculation, the bacterial growth was measured. Bars represent logarithmic units of colony forming units per cm2 of leave. Error bars represent standard deviation (n = 16 plants). The experiments were repeated at least three times with similar results.

JA- but not SA-induced disease resistance against P. syringae is impaired in the ocp3-1 mutant. Two-week-old plants were treated by dipping with a solution of 50 μM MeJA (light grey), 50 μM SA (white) or MgSO4 as control treatment (black). After two days, plants were challenge inoculated as described in Figure 1b. Asterisks indicate significant difference from the control treatment (P < 0.05) using the Student's t test. The experiments were repeated a minimum of three times with similar results.

Mutant ocp3-1 is not JA-insensitive. Effect of JA on Col-0 and ocp3-1 plants. Plants were grown in MS plates supplemented with indicated MeJA concentrations during 10 days. Root growth inhibition was represented as the difference to the control (0 μM MeJA) treatment. (a) Root growth inhibition. Bars represent the JA-induced rooth-growth inhibition in Col-0 (black bars) and ocp3-1 plants (white bars). (b) Anthocyanin accumulation. Lines represent the anthocyanin accumulation in the same experiment. Anthocyanin quantification was performed by a spectrophotometric method. Error bars represent standard deviation (n = 5 plates). The experiments were repeated three times with similar results.

Overexpression of a cytosolic isoform of NPR1 (NPR1-HBD) restores the impaired JA-induced disease resistance in ocp3-1 plants while dexamethasone treatment eliminates this protective effect. (a) Two-week-old plants were treated by dipping with a solution of 10 mM MgSO4 (Control) or 50 μM MeJA. After two days, plants were challenge inoculated as described in Figure 3. Asterisks indicate significant difference from the control treatment (P < 0.05) using the Student's t test. (b) As in (a), plants were treated with 10 mM MgSO4 (Control), with 50 μM MeJA, with 5 μM dexamethasone (DEX) or with 50 μM MeJA plus 5 μM dexamethasone (DEX). The experiments were repeated three times with similar results.